Abstract

Arrays of chemical oxidants are produced in healthy cells, where they function as important signaling molecules that are crucial in homeostatic regulation and cellular adaptation. The molecular basis of “redox signaling” is a series of oxido-reductive chemical reactions in which oxidants or reductants post-translationally alter the structure of proteins. These modifications equate to signal sensing events, in which an alteration in protein redox status may couple to a change in its function. This coupling of sensing to function is a true transduction event, allowing conversion of the cellular redox state into altered enzymatic activities. Here we review redox signaling in the cardiovascular system, considering the variety of post-translational oxidative modifications that explain redox sensing and signal transduction by proteins at the molecular level.